Epicardial Adipose Tissue in Cardiovascular Disease.


Journal

Advances in experimental medicine and biology
ISSN: 0065-2598
Titre abrégé: Adv Exp Med Biol
Pays: United States
ID NLM: 0121103

Informations de publication

Date de publication:
2019
Historique:
entrez: 30 5 2019
pubmed: 30 5 2019
medline: 8 8 2019
Statut: ppublish

Résumé

Cardiovascular disease (CVD) is the main cause of morbidity and mortality in industrialized countries, despite the evolution of treatments and revascularization strategies. Obesity, also accompanied by a chronic inflammatory process, is an independent risk factor for CVD. Abdominal adipose tissue is a complex, metabolically very active organ capable of producing different adipokines and hormones, responsible for endocrine-metabolic comorbidities. The epicardial adipose tissue (EAT) has not been as extensively studied as the abdominal or subcutaneous adipose tissue. However, recent evidence associates it with an increased cardiometabolic risk due to its apposition with the heart. EAT stores triglycerides to provide energy to the myocardium and is characterized by its greater ability to release and capture free fatty acids. EAT strategic localization allows a singular cross talk with cardiomyocytes and vascular wall cells. The fact that EAT produces pro-inflammatory adipokines as well as metalloproteinases and pro-oxidant substances, highlights its possible direct impact on plaque vulnerability and heart failure, being still necessary further studies of EAT behavior in CVD.

Identifiants

pubmed: 31140176
doi: 10.1007/978-3-030-11488-6_9
doi:

Substances chimiques

Adipokines 0
Reactive Oxygen Species 0
Triglycerides 0
Metalloproteases EC 3.4.-

Types de publication

Journal Article Review

Langues

eng

Pagination

131-143

Auteurs

Gabriela Berg (G)

Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica, Cátedra de Bioquímica Clínica I, Laboratorio de Lípidos y Aterosclerosis, Universidad de Buenos Aires, Buenos Aires, Argentina. gaberg@ffyb.uba.ar.
Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC), Universidad de Buenos Aires, Buenos Aires, Argentina. gaberg@ffyb.uba.ar.
CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina. gaberg@ffyb.uba.ar.

Verónica Miksztowicz (V)

Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica, Cátedra de Bioquímica Clínica I, Laboratorio de Lípidos y Aterosclerosis, Universidad de Buenos Aires, Buenos Aires, Argentina.
Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC), Universidad de Buenos Aires, Buenos Aires, Argentina.
CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.

Celina Morales (C)

Facultad de Medicina, Instituto de Fisiopatología Cardiovascular, Departamento de Patología, Universidad de Buenos Aires, Buenos Aires, Argentina.

Magalí Barchuk (M)

Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica, Cátedra de Bioquímica Clínica I, Laboratorio de Lípidos y Aterosclerosis, Universidad de Buenos Aires, Buenos Aires, Argentina.
Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC), Universidad de Buenos Aires, Buenos Aires, Argentina.

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Classifications MeSH